GPX4 and polycystic ovary syndrome: Our data demonstrated intracellular Fe2+ accumulation, ROS release, lipid peroxidation, mitochondrial injury, ferroptosis cargo receptor NCOA4 upregulation, and iron storage protein FTH1 and ferroptosis key suppressor GPX4 loss, which resulted in GC ferroptosis in both PCOS patients and the DHEA-induced PCOS rat model.